Article Text

Download PDFPDF
Lipid-rich environment: a key role promoting carcinogenesis in obesity-related non-alcoholic fatty liver disease
  1. Patricia Aspichueta1,2
  1. 1 Department of Physiology, Faculty of Medicine and Nursing, University of Basque Country UPV/EHU, Leioa, Spain
  2. 2 Biocruces Health Research Institute, Cruces University Hospital, Barakaldo, Spain
  1. Correspondence to Dr Patricia Aspichueta, Department of Physiology, Faculty of Medicine and Nursing, University of the Basque Country UPV/EHU, 48940 Leioa, Spain; patricia.aspichueta{at}ehu.es

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

The epidemic of obesity has led to increased risk of many types of cancer including hepatocellular carcinoma (HCC).1 HCC is the most frequent presentation of liver cancer, the fifth most common cancer in men worldwide and the seventh in women.2 Even though viral and alcohol-related liver diseases are main causes of HCC, non-alcoholic fatty liver disease (NAFLD) has become the most rapidly increasing cause during the last decade.1 Even more, HCC may also develop in the absence of liver cirrhosis, and the incidence in livers without fibrosis is higher in the metabolic syndrome and NAFLD.1 According to data from the Surveillance, Epidemiology and End Results registries (2004–2009), in the USA, NAFLD-driven HCC is associated with shorter survival time and more advanced tumour stage.3 Besides, although numerous drugs have been proposed, there is still no available treatment for most patients with HCC.4 Thus, there is a need to understand the mechanism involved in NAFLD-driven HCC to provide new targets of treatment. A hallmark of NAFLD and HCC is the disrupted lipid metabolism. Fujiwara et al 5 provide a new mechanism that links lipid accumulation with carcinogenesis in …

View Full Text

Footnotes

  • Contributors PA wrote the commentary.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

Linked Articles